Where it comes from
- Made in
- A few hypothalamic neurons (ventromedial and lateral), plus testis and fat; its receptor sits in retina and bone
- Sent out by
- Fasting raises it
- Acts on
- Hypothalamic feeding circuits
- Osteoblasts
- Islets (insulin)
- Fat cells
- Adrenal (aldosterone)
What it does
- Drives feeding and fat storage when given centrally; mice held to a matched ration still gained fat 1
- Mice lacking its receptor have thin bones, and the peptide releases aldosterone from adrenal cells 3
- Part of the brain’s long-term control of body weight; its neurons drive a hibernation-like state in mice, though the peptide itself is not needed for that 2
In medicine
- No medicine copies it or blocks it, and it is not measured in people
- Its receptor has no ligand in clinical use. The interest in it is in bone and in body weight, and both rest on mouse work 3
Beyond the body’s own use
- Nothing containing it is in trials, approved or obtainable outside the laboratory
- Its neurons are the striking part. Switching them on drops a mouse into a hibernation-like state, with body temperature and metabolic rate down for days; mice that cannot make the peptide still do it, so the circuit rather than the peptide carries the effect 2
- What is unknown is which of the gene’s two peptides does the work. QRFP-43 and 26RFa act at the same receptor, and nearly all the feeding and glucose work uses the shorter one 3
Sources
- Takayasu et al., A neuropeptide ligand of GPR103 regulates feeding, arousal and blood pressure in mice, PNAS 2006
- Takahashi et al., A discrete neuronal circuit induces a hibernation-like state in rodents, Nature 2020
- Leprince et al., The RF-amide peptide 26RFa and its receptor, IUPHAR Review 24, British Journal of Pharmacology 2017
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.